title: Molecular Evidence of Injury and Inflammation in Normal and Fibrotic Renal Allografts One Year Post-Transplant

status: Public on Mar 30 2007

first: Walter

last: Park

summary:
Introduction.  Factors contributing to kidney transplant fibrosis remain incompletely understood—particularly in the absence of acute complications.
Methods.   Baseline and one-year surveillance biopsies from 15 uncomplicated living donor kidney transplants were subjected to microarray and quantitative RT-PCR (qRT-PCR) analyses in order to examine changes in gene expression patterns over time. Biopsy pairs were purposefully selected from allografts with no history of acute complications and were divided into those that were histologically normal (n = 7) and those that had developed subclinical interstitial fibrosis (n = 8) at 1 year.
Results.   Compared to the paired baseline specimens, expression levels of 3578 probesets were found altered in all the one-year biopsies studied. A large proportion of the upregulated genes in this transplant-associated profile were functionally linked with inflammation, immunity or response to injury. These included components of inflammation-related signaling pathways (integrin, interferon and TLR) as well as individual mediators of inflammatory and immune responses. An additional 2884 probesets demonstrated altered expression in fibrotic grafts only at 1 year. The gene products in this fibrosis-associated profile were also predominantly linked with inflammation and immune function, suggesting exaggerated inflammatory activity within the fibrotic grafts. qRT-PCR analyses confirmed the predicted expression patterns for selected transcripts from the microarray profiles.
Conclusions.   Transcriptional profiles of histologically normal living donor renal allografts indicate that there is ongoing injury response and inflammation at 1 year compared to the immediate post-transplant period. Subclinical development of interstitial fibrosis during the first post-transplant year is associated with additional upregulation of inflammation-related genes.
Keywords: time course, comparative expression

overall_design: We analyzed gene expression from a group of 15 renal transplant patients.  All patients had histologically normal time zero biopsy but while 7 remained histologically normal (TxNorm), 8 developed subclinical interstitial fibrosis (GIF/TA) by 1 year.  Patient groups were carefully selected to include patients on the same immunosuppresion therapy, transplant type, biopsy histology and absence of overt post-transplant complications (acute rejection, BK, etc).

first: Matthew

last: Griffin

first: Joseph

middle: P

last: Grande

first: Fernando

last: Cosio

first: Mark

last: Stegall


title: Yersinia pseudotuberculosis ymoA mutant vs. wild type YPIII

status: Public on Jul 31 2012

city: Braunschweig

first: Ann

middle: Kathrin

last: Heroven

state: Niedersachsen

address: Inhoffenstr. 7

department: Molecular Infection Biology

country: Germany

institute: Helmholtz Centre for Infection Research

summary: Expression of the virulence regulator RovA of Yersinia pseudotuberculosis, is controlled by the ncRNAs CsrB and CsrC through CsrA and RovM. In this study, we show that the regulator YmoA of the Hha family of nucleoid-associated proteins controls expression of the counterregulated Csr-type RNAs and the Csr-RovM-RovA signalling cascade through alterations of the CsrC RNA stability. YmoA-mediated stabilization of CsrC depends on CsrA and H-NS, but not on the RNA chaperone Hfq and involves a stabilizing stem-loop structure within the 5’-region of CsrC. YmoA influence on CsrC stability is complex as YmoA was found to control numerous factors known to affect RNA structures and stability. In addition, YmoA controls temperature-dependent early and later stage virulence genes in an opposite manner and coregulates their expression with bacterial stress responses and metabolic functions. Following oral infections in a mouse model, we demonstrate that a ymoA mutant is strongly reduced in its ability to disseminate to the Peyer’s patches, mesenteric lymph nodes, liver and spleen and exhibits a reduced mortality. We propose a model in which YmoA controls switching from a RovA-dependent early colonization phase towards a virulence plasmid (pYV)-dependent infection phase important for host defense and persistence.

overall_design: For each microarray, 300ng of each Cy3- and Cy5-labelled RNA were mixed, fragmented and hybridized to the microarray at 65°C for 17 hours using the Agilent Hybridization Chamber according to the Agilent instructions. Four replicates were performed. Sequences used for the design of the microarray (Agilent, 8 x 15K format) include three different 60-nt oligonucleotides for all 4172 chromosomal genes (ORFs > 30 codons) of the Y. pseudotuberculosis YPIII genome and six probes for the 92 genes of the virulence plasmid pYV of Y. pseudotuberculosis strain IP32953.

middle: K

first: Katja

last: Böhme

first: Petra

last: Dersch

first: Johannes

last: Klein

first: Richard

last: Münch

first: Jana

last: Melzer


title: Tbr1 regulates regional and laminar identity of postmitotic neurons in developing neocortex

status: Public on Jul 27 2010

city: Seattle

first: James

middle: William

last: MacDonald

state: WA

address: 4225 Roosevelt Way NE

department: Environmental and Occupational Health Sciences

country: USA

institute: University of Washington

summary: Areas and layers of the cerebral cortex are specified by genetic programs that are initiated in progenitor cells and then, implemented in postmitotic neurons. Here, we report that Tbr1, a transcription factor expressed in postmitotic projection neurons, exerts positive and negative control over both regional (areal) and laminar identity. Tbr1 null mice exhibited profound defects of frontal cortex and layer 6 differentiation, as indicated by down-regulation of gene-expression markers such as Bcl6 and Cdh9. Conversely, genes that implement caudal cortex and layer 5 identity, such as Bhlhb5 and Fezf2, were up-regulated in Tbr1 mutants. Tbr1 implements frontal identity in part by direct promoter binding and activation of Auts2, a frontal cortex gene implicated in autism. Tbr1 regulates laminar identity in part by downstream activation or maintenance of Sox5, an important transcription factor controlling neuronal migration and corticofugal axon projections. Similar to Sox5 mutants, Tbr1 mutants exhibit ectopic axon projections to the hypothalamus and cerebral peduncle. Together, our findings show that Tbr1 coordinately regulates regional and laminar identity of postmitotic cortical neurons.

overall_design: Mouse E14.5 neocortices and Postnatal day (P) 0.5 brains: E14.5 neocortices KO, 3; E14.5 neocortices WT, 3; Postnatal day (P) 0.5 brains frontal WT, 4; Postnatal day (P) 0.5 brains frontal KO, 4; Postnatal day (P) 0.5 brains parietal WT, 4; Postnatal day (P) 0.5 brains parietal KO, 4; Postnatal day (P) 0.5 brains occipital WT, 4; Postnatal day (P) 0.5 brains occipital KO, 4.

last: Beyer

first: Francesco

last: Bedognia

first: Rebecca

middle: D

last: Hodgea

first: Gina

middle: E

last: Elsena

first: Branden

middle: R

last: Nelson

first: Ray

middle: A

last: Dazaa

first: John

middle: L

last: Rubensteind

first: Robert

middle: F

last: Hevner


title: An Omics based meta-analysis to support infection state stratification [Illumina dataset]

status: Public on Dec 08 2020

city: London

first: ashleigh

last: Myall

address: Exhibition Rd, South Kensington, London

country: United Kingdom

institute: Imperial College London

type:
Third-party reanalysis
Expression profiling by array

summary: A fundamental problem for disease treatment is that while antibiotics are a powerful counter to bacteria, they are ineffective against viruses. Often, bacterial and viral infections are confused due to their similar symptoms and lack of rapid diagnostics. With many clinicians relying primarily on symptoms for diagnosis, overuse and misuse of modern antibiotics are rife, contributing to the growing pool of antibiotic resistance. To ensure an individual receives optimal treatment given their disease state and to reduce over-prescription of antibiotics, the host response can in theory be measured quickly to distinguish between the two states. To establish a predictive biomarker panel of disease state (viral/bacterial/no-infection) we conducted a meta-analysis of human blood infection studies using Machine Learning (ML). We focused on publicly available gene expression data from two widely used platforms, Affymetrix and Illumina microarrays as they represented a significant proportion of the available data. We were able to develop multi-class models with high accuracies with our best model predicting 93% of bacterial and 89% viral samples correctly. To compare the selected features in each of the different technologies, we reverse engineered the underlying molecular regulatory network and explored the neighbourhood of the selected features. The networks highlighted that although on the gene-level the models differed, they contained genes from the same areas of the network. Specifically, this convergence was to pathways including the Type I interferon Signalling Pathway, Chemotaxis, Apoptotic Processes, and Inflammatory / Innate Response.

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Reanalysis of: GSM992800
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Reanalysis of: GSM992802
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Reanalysis of: GSM812751
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Reanalysis of: GSM812659
Reanalysis of: GSM812676
Reanalysis of: GSM812655
Reanalysis of: GSM812688
Reanalysis of: GSM812689
Reanalysis of: GSM812690
Reanalysis of: GSM812702
Reanalysis of: GSM812699
Reanalysis of: GSM1668107
Reanalysis of: GSM1668113
Reanalysis of: GSM1667382
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Reanalysis of: GSM1667690
Reanalysis of: GSM1667691
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Reanalysis of: GSM1667422
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Reanalysis of: GSM1667697
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Reanalysis of: GSM1667700
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Reanalysis of: GSM1667876
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Reanalysis of: GSM1668146
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Reanalysis of: GSM1667683
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Reanalysis of: GSM1667896
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Reanalysis of: GSM1667900
Reanalysis of: GSM1668147
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Reanalysis of: GSM1667440
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Reanalysis of: GSM1667708
Reanalysis of: GSM1667709
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Reanalysis of: GSM1667713
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Reanalysis of: GSM1667902
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Reanalysis of: GSM1667908
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overall_design:
The study is a batch corrected combination of several study datasets. Partial sample description (GSE,GPL,GSM,organism, and sample type) are provided (in the re-analyzed_sample_reference.txt) as all data is coming from pre-published studies and can be found using the sample references provided.
1751 samples from published studies (including bacterial(b,b?), viral(v,v?), and control(c) samples) combined, batch corrected and then analysed following the outlined methods in https://www.medrxiv.org/content/10.1101/2020.07.28.20163329v2

first: Ashleigh

first: Simon

last: Perkins

first: David

last: Rushton

first: Jonathan

last: David

first: Phillippa

last: Spencer

first: Andrew

last: Jones

first: Philipp

last: Antczak


title: An Omics based meta-analysis to support infection state stratification [Affymetrix dataset]

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overall_design:
The study is a batch corrected combination of several study datasets. Partial sample description (GSE,GPL,GSM,organism, and sample type) are provided (in the re-analyzed_sample_reference.txt) as all data is coming from pre-published studies and can be found using the sample references provided.
1676 samples from published studies (including bacterial(b,b?), viral(v,v?), and control(c) samples) combined, batch corrected and then analysed following the outlined methods in https://www.medrxiv.org/content/10.1101/2020.07.28.20163329v2